STROKE INTRODUCTION, CLASSIFICATION AND CLINICAL FEATURES.pptx

This presentation can be reffered by final year BPTh, MBBS, NURSING students for better understanding of stroke.

1. DEPARTMENT OF NEUROSCIENCES. DATTA MEGHE COLLEGE OF PHYSIOTHERAPY. Nagpur.

2. STROKE (INTRODUCTION, CLASSIFICATION AND CLINICAL FEATURES) DR. NEHA INGALE CHAUDHARY MPT (Neuro) PROFESSOR & HEAD DR. SACHIN CHAUDHARY MPT (Cardio- respi . Physiotherapy) PROFESSOR & HEAD DATTA MEGHE COLLEGE OF PHYSIOTHERAPY. Nagpur.

3. PREFACE This PPT is intended primarily for Bachelor of Physiotherapy (BPTh) Final year students those are under preparation for their University Examination. I have attempted to cover different areas of stroke. Despite my best efforts there might have some errors. I like to thank all those who have helped me. Dr. Neha Ingale Chaudhary Dr. Sachin Chaudhary

4. CONTENT Sr. No. Topic Slide No 1 Objectives 5- 6 2 Introduction of stroke and Transient Ischemic Stroke. 9-11 3 Epidemiology , Etiology , Risk factors and warning signs 12-17 4 Pathophysiology 18-19 5 Classification and syndromes 20-33 6 Red flags 33 7 Clinical features 34-55 8 Investigations and Prognosis 56-59 9 Summary 60 10 References 61 11 Questions 62

5. GENERAL OBJECTIVES OF THE SYLLABUS At the end of the session student should be able to understand – The definition, epidemiology, Pathophysiology, and classification of stroke. The clinical features and the investigations done for stroke. The investigations and prognosis outcome of stroke.

6. LEARNING OBJECTIVES Sr. no Learning objectives domain level criteria 1 Explain Stroke, etiology, Pathophysiology. Cognitive Must know All 2 Explain different types and syndromes of Stroke. Cognitive & Psychomotor Must know A ll 3 Explain clinical features of stroke Cognitive & Psychomotor Must know All 4 Explain investigations required and prognostic features of stroke Cognitive & Psychomotor Must know All

7. CHAPTER CONTENT Sr. No. Topic Slide No 1 Introduction 5- 6 2 Transient ischemic attack 9-11 3 Epidemiology , Etiology , Risk factors and warning signs 12-17 4 Pathophysiology 18-19 5 Classification and syndromes 20-32 6 Red flags 33 7 Clinical features 34-55 8 Investigations and Prognosis 56-59

8. INTRODUCTION AND CLASSIFICATION STROKE

9. INTRODUCTION Stroke is an acute onset of neurological dysfunction due to an abnormality in cerebral circulation with resultant signs & symptoms which corresponds to involvement of focal areas of the brain

10. ACC. TO WHO It is defined as the sudden onset of neurological deficits due to an abnormality in cerebral circulation with the signs and symptoms lasting for more than 24 hours or longer

11. TRANSIENT ISCHEMIC ATTACK It is defined as the sudden onset of neurological deficits due to an abnormality in cerebral circulation with the signs and symptoms lasting for less than 24 hours

12. EPIDEMIOLOGY Third leading cause of death The incidence of stroke is about 1.25 times greater for males than females Most common cause of disability among adults

13. ETIOLOGY Atherosclerosis. Cerebral Thrombus. Cerebral embolus. Embolism from the heart (cardiac origin) Intracranial hemorrhage. Subarachnoid hemorrhage. Intracranial small vessel disease. Arterial aneurysms and Arterio-venous malformation. Haematological disorders (haemoglobinopathies, leukemia) Atherothromboembolism

14. MISCELLANEOUS RARE CAUSES OF STROKE Infective endocarditis & HIV infection Tumour, Hypoglycemia, Chronic meningitis Perioperative stroke (hypotension and boundary zone infarction, trauma, dissection of neck arteries, paradoxical embolism, fat embolism, infective endocarditis) Migraine, Snake bite Inflammatory bowel disease (Ulcerative and Crohn's colitis)

15. RISK FACTORS Smoking Obesity Lack of physical exercise or sedentary life style Diet & excess alcohol consumption Oral contraceptives Infection (meningeal infection) Psychological factors Vasectomy Ageing & gender Positive family history Circadian and seasonal factors Heart disease Diabetes mellitus Hypertension Peripheral arterial disease Blood pathology Hyperlipidemia , TIA Non Modifiable Modifiable

16. STROKE EARLY WARNING SIGN F- Face Drooping A- Arm Weakness S- Speech Difficulty T- Time To Call Hospital

17. OTHER THAN FAST SIGN- Sudden Weakness, Numbness Of Leg Sudden Confusion Or Trouble In Understanding Sudden Trouble In Seeing or Walking Sudden Severe Headache With No Known Cause Other important but less common stroke symptoms include: Sudden nausea, fever, & vomiting distinguished from a viral illness by speed of onset Brief loss of consciousness (fainting, confusion, convulsions)

18. PATHOPHYSIOLOGY Ischemia results in irreversible cellular damage with a core area of focal infarction within minutes Transitional area surrounding core is termed ischemic penumbra & consists of viable but metabolically lethargic cells Ischemia produce cerebral edema , that begins within minutes of insult & reaches a maximum by 3 to 4 days.

19. Swelling gradually subsides & generally disappears by 2 - 3 weeks. Edema elevates ICP, leading to intracranial HT & neurological deterioration associated with contra lateral & caudal shifts of brain structures. Cerebral edema is the most frequent cause of death in acute stroke & is characteristic of large infarcts involving MCA & ICA.

20. CLASSIFICATION Depending on the cause Hemorrhagic stroke Intracranial hemorrhage Subarachnoid hemorrhage Signs of raised ICP will be evident with a history of a traumatic accident

21. Contd… Ischemic stroke Thrombotic: more common. Usually occurs in the sleeping hours. Characterized by gradual onset of symptoms Embolic: Occurs in the waking hours of the day. Sudden onset of symptoms preceded by giddiness in most conditions

22. Depending on the severity Mild stroke : symptoms subside with no deficit in a week period. Moderate stroke : symptoms recover in a period of 3 - 6 months with minimal neurological deficit. Severe stroke : no complete recovery of the symptoms, even after 1 year. Always ends up with severe neurological deficit.

23. Depending on the duration Acute stroke : to a period of one week or until spasticity develops Sub acute stroke : after the development of spasticity & last for a period of 3-12 months Chronic stroke : more than 12 months

24. Depending on the artery involved- Depending on the artery involved- MCA Syndrome ACA Syndrome PCA syndrome Vertebro basilar artery syndrome Vertebral, basilar artery Internal carotid artery Lacunar syndrome

25. MCA SYNDROME Contralateral hemiplegia (UL & face >LL) Contralateral hemi sensory loss (UL & face more affected than LL) Ideomotor apraxia Ataxia of contra lateral limb Contralateral Homonymous hemianopia Left hemisphere infarction Contralateral neglect Possible Contralateral visual field deficit Aphasia: Broca’s (expressive) or Wernicke’s (receptive)

26. ACA SYNDROME Contralateral Hemiplegia or monoplegia of LL (LL >UL) Contralateral sensory loss of LL Urinary incontinence Problems with imitation & bimanual task Abulia ( akinetic mutism ) Apraxia Amnesia Contralateral grasp reflex, sucking reflex

27. PCA SYNDROME Coordination disorders such as tremor or ataxia Contralateral homonymous field deficit Cortical blindness Cognitive impairment including memory impairment Contralateral sensory impairment Thalamic syndrome (severe pain from touch or temp. changes) Weber’s syndrome (Contralateral hemiplegia & third nerve palsy)

28. VERTIBRO-BASILAR ARTERY SYNDROMES Medial medullary syndrome (VA) Lateral medullary (Wallenberg's) syndrome (PICA) Complete basilar artery syndrome (locked-in syndrome) Med inferior pontine syndrome Lateral inferior pontine syndrome (AICA) Medial midpontine syndrome Lateral midpontine syndrome Medial superior pontine syndrome Lateral superior pontine syndrome

29. Locked-in syndrome (LIS) Acute hemiparesis rapidly progressing to tetraplegia & lower bulbar paralysis (CN V through XII are involved) Initially patient is dysarthric & dysphonic & progresses to mutism There is preserved consciousness & sensation Horizontal eye movements are impaired but vertical eye movements & blinking remain intact. Communication can be established via these eye movements.

30. LACUNAR SYNDROME Caused by small vessel disease of deep white mater Pure motor Lacunar stroke Pure sensory Lacunar stroke Ataxic hemiparesis Dysarthria Clumsy hand syndrome Sensory/motor stroke Dystonia/involuntary movements

31. RED FLAG Changes in neurological status Symptoms Possible causes Management Decreased level of arousal enlargement of pupil on the side of stoke sudden change in muscle tone and /or deep tendon reflexes Cerebral edema Another attack of stroke Cease treatment and seek immediate medical attention

32. CLINICAL FEATURES AND INVESTIGATIONS OF STROKE.

33. PRIMARY IMPAIRMENT 1. Altered sensation Pain (central pain or thalamic pain syndrome) characterized by constant, severe burning pain with intermittent sharp pains Hyperalgesia Loud sound, bright light etc. may trigger pain

34. 2 . Vision Homonymous hemianopia, a visual field defect, occurs with lesions involving the optic radiation (MCA) or to primary visual cortex (PCA) Visual neglect & problems with depth perception, and spatial relationships

35. 3. Weakness Usually seen in the contralateral side of the lesion MCA stroke are more common so weakness is largely seen in the UL in clinical practice Distal muscle are more affected than proximal muscles Mild weakness of ipsilateral side

36. 4. Alteration of tone Flaccidity (hypotonicity) is present immediately after stroke also called as cerebral shock. Spasticity (hypertonicity) emerges in about 90 percent of cases

37. 5. Abnormal synergy Extremity Flexion synergy components Extensor synergy components Upper extremity Scapular retraction/elevation or hyperextension Shoulder abduction, external rotation Elbow flexion* Forearm supination Wrist and finger flexion Scapular protraction Shoulder adduction*, internal rotation Elbow extension Forearm pronation* Wrist and finger flexion Lower extremity Hip flexion*, abduction, external rotation Knee flexion Ankle dorsiflexion , inversion Toe dorsiflexion Hip extension, adduction*, internal rotation Knee extension* Ankle plantarflexion*, eversion Toe plantarflexion

38. Muscles not involved in either synergy Latissimus dorsi Teres major Serratus anterior Finger extensors Ankle evertors

39. 6. Abnormal reflexes Initially, hyporeflexia with flaccidity & later hyperreflexia Clonus, & positive Babinskie Asymmetric tonic neck reflex (ATNR) present most of times. Associated reactions are also present by stimulation of yawning, sneezing, or coughing.

40. 7. Altered co ordination Proprioceptive loss can result in sensory ataxia. Strokes affecting cerebellum typically produce cerebellar ataxia (e.g. Basilar Artery Syndrome, Pontine Syndromes) & motor weakness. Basal ganglia involvement (PCA syndrome) may lead to bradykinesia or involuntary movements.

41. 8. Altered motor programming Lesions of premotor frontal cortex of either hemisphere, left inferior parietal lobe, & corpus callosum can produce Apraxia. Apraxia is more evident with left hemisphere damage than right and is commonly seen with aphasia. Ideational apraxia Ideomotor apraxia

42. 9. Postural Control & Balance Impairments in steadiness, symmetry, & dynamic stability. Reactive postural control and Anticipatory postural control affected. Pusher syndrome: A ctive pushing with stronger extremities toward affected side, leading to lateral postural imbalance.

43. 10. Speech, Language, and Swallowing Lesions of dominant hemisphere. Aphasia: impairment of language comprehension, formulation, and use. D ysarthria: M otor speech disorders -lesions of CNS or PNS. D ysphagia: L esions affecting medullary brainstem (CN IX and X), large vessel pontine lesions, acute MCA and PCA lesion

44. 11. Perception and Cognition Disorders of body scheme/body image , spatial relations , and agnosias . Result of lesions in right parietal cortex & seen more with left hemiplegia than right.

45. 12. Emotional Status Pseudobulbar affect (PBA) , also known as emotional liability or emotional dysregulation syndrome. emotional outbursts or exaggerated laughing or crying. Lesions of brain affecting frontal lobe, hypothalamus, & limbic system Depression is extremely common

46. 13. Bladder and Bowel Function Common during acute phase. Urinary incontinence- bladder hyperreflexia or hyporeflexia, loss of sphincter control, or sensory loss. Bowel function affection: Incontinence & Diarrhea or Constipation

47. HEMISPHERIC BEHAVIORAL DIFFERENCES

48. INDIRECT IMPAIRMENTS 1. Musculoskeletal changes Loss of ROM & Contractures. Disuse atrophy & muscle weakness. Osteoporosis, results from decreased physical activity, changes in protein nutrition, hormonal deficiency, & calcium deficiency.

49. 2. Neurological signs Seizures occur in a small % of patients - more common in occlusive carotid disease than in MCA disease Hydrocephalus - rare but can occur with subarachnoid or intracerebral hemorrhage.

50. 3. Thrombophlebitis & deep venous thrombosis (DVT) Commonest complications for all immobilized patients.

51. 4. Cardiac Function Stroke as a result of underlying coronary artery disease (CAD) -impaired CO, cardiac decompensation , & rhythm disorders. If problems persist, can alter cerebral perfusion & produce additional focal signs (e.g., mental confusion). Cardiac limitations in exercise tolerance

52. 5. Pulmonary Function Decreased lung volume, decreased pulmonary perfusion & vital capacity & altered chest wall excursion Aspiration- due to Dysphagia.

53. 6. Integumentary Pressure sore/ decubitus ulcer. Fragile skin- reduced blood supply to epidermis. The skin breaks down over bony prominences from pressure, friction, shearing, and/or maceration

54. TESTS AND MEASURES Urine analysis CBC count Blood sugar level Blood cholesterol & lipid profile Cardiac evaluation Lumbar puncture

55. IMAGING CT Scan. Magnetic Resonance Imaging (MRI). Cerebral Angiography.

56. RECOVERY AND PROGNOSIS Fastest in first weeks after onset Measurable neurological & functional recovery – in first month after stroke. Continue to make measurable functional gains for months or years after insult. Late recovery of function- seen in patients with chronic stroke undergoing extensive functional training

57. VARIATION OF RECOVERY Recovery depends on severity of stroke . Depends on type of stroke – hemorrhagic or ischemic. Varies from individual to individual. Depends on intensity of therapy. Depends on age of the patient.

58. SUMMARY Introduction Etiology, epidemiology Risk factors, warning signs Pathophysiology, syndromes Clinical features Investigations and prognosis

59. REFERENCES O’ Sullivan SB, Schmitz TJ. Stroke. Physical rehabilitation. 7 th ed., New Delhi: Jaypee Brothers, 2007, chapter 15, P(592-661) Darcy A. Umphred. Neurological Rehabilitation, 6 th ed., Mosby Elsevier, Missouri.Chapter 23, P(711-752).

60. QUESTIONS Define stroke and explain causes. Describe various syndromes occurring in stroke. Illustrate various clinical features and prognosis of stroke

61. Thank you…